Current obesity reports · 2026
Obesity-Associated Osteoarthritis: Mechanical-Metabolic Pathogenesis, Obesity Memory and Dual-Target Therapy.
СтатьяОбзорНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Wang Yudan, Fan Xinhao, Gao Jingyuan, Xing Lei, Tian Faming
Аннотация
PURPOSE OF REVIEW: Given the global obesity epidemic, osteoarthritis (OA) incidence is expected to rise, posing a substantial public health burden. This review covers epidemiological associations of obesity and OA, controversial mechanisms, and current prevention and treatment limitations. Based on these insights, we propose a dual‑target treatment strategy for obesity‑induced OA.
RECENT FINDINGS: Leptin signaling and mechanical overload from excess adiposity independently drive OA pathogenesis, whereas obesity‑related adipose dysfunction exerts its pathogenic effects only in the presence of mechanical loading. Obesity‑induced residual memory may persist and sustain joint damage even after weight loss and metabolic improvement. Evidence‑based weight loss strategies should be implemented to prevent OA, with the preventive window for obesity shifting to infancy. Given the limited and controversial structural benefits of current clinical interventions, a dual‑target strategy combining weight loss with memory‑targeted interventions is warranted. This review provides new insights into the debate on mechanical versus metabolic mechanisms in obesity‑induced OA, clarifying their relative contributions. Earlier obesity prevention interventions offer a broader window for OA prevention. Given these limitations, a dual‑target strategy addressing both excessive fat accumulation and its persistent adverse effects may represent a promising clinical direction, with particular potential for repurposing FDA‑approved agents such as semaglutide and metformin in this context.
RECENT FINDINGS: Leptin signaling and mechanical overload from excess adiposity independently drive OA pathogenesis, whereas obesity‑related adipose dysfunction exerts its pathogenic effects only in the presence of mechanical loading. Obesity‑induced residual memory may persist and sustain joint damage even after weight loss and metabolic improvement. Evidence‑based weight loss strategies should be implemented to prevent OA, with the preventive window for obesity shifting to infancy. Given the limited and controversial structural benefits of current clinical interventions, a dual‑target strategy combining weight loss with memory‑targeted interventions is warranted. This review provides new insights into the debate on mechanical versus metabolic mechanisms in obesity‑induced OA, clarifying their relative contributions. Earlier obesity prevention interventions offer a broader window for OA prevention. Given these limitations, a dual‑target strategy addressing both excessive fat accumulation and its persistent adverse effects may represent a promising clinical direction, with particular potential for repurposing FDA‑approved agents such as semaglutide and metformin in this context.